TY - JOUR
T1 - Do vestibular otolith organs participate in human orthostatic blood pressure control?
AU - Watenpaugh, Donald E.
AU - Cothron, Adriena V.
AU - Wasmund, Stephen L.
AU - Wasmund, Wendy L.
AU - Carter, Robert
AU - Muenter, Nicolette K.
AU - Smith, Michael L.
N1 - Funding Information:
We thank the subjects for their participation, and Debbie Castillo for administrative assistance. This work was supported in part by the United States National Aeronautics and Space Administration grant NAG 5-3744, and by a National Medical Fellowship from Bristol Myers Squibb, to Adriena Cothron.
PY - 2002/9/30
Y1 - 2002/9/30
N2 - We hypothesized that vestibular otolith organ stimulation contributes to human orthostatic responses. Twelve subjects underwent three 60° upright tilts: (1) with the neck flexed from 0° to 30° relative to the body during 60° tilt, such that the head moved from horizontal to 90° above horizontal (0 to 1 Gz otolith stimulation); (2) with the head and body aligned, such that they tilted together to 60° (0 to 0.87 Gz otolith stimulation); and (3) with the neck flexed 30° relative to the body during supine conditions, and the neck then extended to -30° during 60° body tilting, such that the head remained at 30° above horizontal throughout body tilting (constant 0.5 Gz otolith stimulation). All three tilt procedures increased thoracic impedance, sympathetic nerve activity (N=8 of 12), arterial pressure, and heart rate relative to supine conditions (all P<0.04). Within the first 20 s of tilt, arterial pressure increased most obviously in the 0 to 1 Gz otolith condition. Thoracic impedance tended to increase more in otolith-constant conditions, but no dependent variable differed significantly between tilt conditions, and no significant time×tilt interactions emerged. Otolith inputs may contribute to early transient adjustments to orthostasis. However, lack of significant main effects of tilt condition and time×tilt interactions suggests that potential otolith effects on the variables we studied are relatively subtle and ephemeral, or that other mechanisms compensate for a lack of change in otolith input with orthostasis.
AB - We hypothesized that vestibular otolith organ stimulation contributes to human orthostatic responses. Twelve subjects underwent three 60° upright tilts: (1) with the neck flexed from 0° to 30° relative to the body during 60° tilt, such that the head moved from horizontal to 90° above horizontal (0 to 1 Gz otolith stimulation); (2) with the head and body aligned, such that they tilted together to 60° (0 to 0.87 Gz otolith stimulation); and (3) with the neck flexed 30° relative to the body during supine conditions, and the neck then extended to -30° during 60° body tilting, such that the head remained at 30° above horizontal throughout body tilting (constant 0.5 Gz otolith stimulation). All three tilt procedures increased thoracic impedance, sympathetic nerve activity (N=8 of 12), arterial pressure, and heart rate relative to supine conditions (all P<0.04). Within the first 20 s of tilt, arterial pressure increased most obviously in the 0 to 1 Gz otolith condition. Thoracic impedance tended to increase more in otolith-constant conditions, but no dependent variable differed significantly between tilt conditions, and no significant time×tilt interactions emerged. Otolith inputs may contribute to early transient adjustments to orthostasis. However, lack of significant main effects of tilt condition and time×tilt interactions suggests that potential otolith effects on the variables we studied are relatively subtle and ephemeral, or that other mechanisms compensate for a lack of change in otolith input with orthostasis.
KW - Gravity
KW - Head-up tilt
KW - Heart rate
KW - Hemodynamics
KW - Muscle sympathetic nerve activity
UR - http://www.scopus.com/inward/record.url?scp=0037201179&partnerID=8YFLogxK
U2 - 10.1016/S1566-0702(02)00142-X
DO - 10.1016/S1566-0702(02)00142-X
M3 - Article
C2 - 12422963
AN - SCOPUS:0037201179
SN - 1566-0702
VL - 100
SP - 77
EP - 83
JO - Autonomic Neuroscience: Basic and Clinical
JF - Autonomic Neuroscience: Basic and Clinical
IS - 1-2
ER -